Heart failure is a syndrome caused by a variety of conditions such as coronary artery disease, hypertension, valve disease, myocarditis and others. Common symptoms of heart failure include shortness of breath, coughing under exertion, swelling of appendages, and dizziness. Heart failure is better defined as the progressive inability of the heart ventricles to pump blood out to the lungs and/or the extremities. Heart failure is
either systolic or diastolic or a combination of both. Severity is usually classified into four classes defined by the New York Heart Association (NYHA class I-IV).
BNP is one member of the family of natriuretic peptides that were initially discovered by de Bold, et al. Although BNP was first isolated from porcine brain tissue (originally named brain natriuretic peptide), the heart has been determined to be the major source. BNP is synthesized and released into the blood in response to volume overload or conditions that cause ventricular stretch, to control fluid and electrolyte homeostasis by interaction with the renin-angiotensin-aldosterone system (RAAS).
PreproBNP (134 amino acids) is synthesized in the cardiac myocytes and is processed to a proBNP (108 amino acids) precursor molecule. TheproBNP is subsequently cleaved into physiologically active BNP (32 aminoacids), and a degradation fragment NT-proBNP (76 amino acids). BNP, NT-proBNP, and a higher molecular weight form have been detected in peripheral blood. BNP is cleared from the circulation, with a half-life (t½) of approximately 23 minutes, by specific cellular receptors and neutral endopeptidases. Numerous studies have indicated that BNP can be used for patient diagnosis, prognosis and therapy monitoring. Levels of BNP have been shown to be elevated in patients with cardiac dysfunction.
Plasma BNP levels provide clinically useful information concerning the diagnosis and management of left ventricular dysfunction and heart failure, which complements other diagnostic testing procedures (e.g.,
electrocardiograms, chest x-rays, and echocardiograms). BNP levels can be used to assess the severity of heart failure, as demonstrated by the correlation with New York Heart Association classifications. Plasma BNP
levels also increase with decreasing physiological functional capacities, as measured by left ventricular ejection fraction (LVEF) or exercise-based evaluations. The European Society of Cardiology has included the use of natriuretic peptides (e.g., BNP) testing in their guidelines for the diagnosis or rule out of heart failure.
Others have suggested that BNP has utility in the stratification of patients with heart failure and acute coronary syndrome (ACS). Elevated levels of BNP in heart failure patients predict disease progression and increased morbidity and mortality. Studies also suggest ACS patients with increased BNP levels have a higher rate of cardiac complications and higher mortality post myocardial infarction. Preliminary studies have reported the use of BNP measurements to optimize patient treatment / management for heart failure. Nesiritide (Natrecor), recombinant BNP has been used for treatment in patients with acute, decompensated heart failure. The efficacy of BNP monitoring, pre- and post-treatment with Natrecor, has been studied. Measurements of BNP two hours or more post-treatment detect only the endogenous levels of BNP.
Manufacturer’s Reagent package insert Architect BNP, November 2015, Abbott Laboratories, Diagnostic Division, Abbott Park IL 60064 USA.